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Weakness

"Asthenia" redirects here. The tortrix moth genus is considered a junior synonym of Epinotia.
Weakness
Classification and external resources
Specialty Neurology
ICD-10 R53
ICD-9-CM 728.87 (728.9 before 10/01/03); alternatively, 780.79
DiseasesDB 22832
MedlinePlus 003174
MeSH D018908

Weakness or asthenia is a symptom of a number of different conditions.[1] The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis.

Contents

  • Differential diagnosis 1
    • True vs. perceived weakness 1.1
    • Asthenia vs. myasthenia 1.2
    • Types 1.3
      • Central fatigue 1.3.1
      • Neuromuscular fatigue 1.3.2
      • Peripheral muscle fatigue 1.3.3
      • Lactic acid hypothesis 1.3.4
  • Pathophysiology 2
  • References 3
  • External links 4

Differential diagnosis

True vs. perceived weakness

  • True weakness (or neuromuscular) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy.
  • Perceived weakness (or non-neuromuscular) describes a condition where a person feels more effort than normal is required to exert a given amount of force but actual muscle strength is normal, for example chronic fatigue syndrome.[2]

In some conditions, such as myasthenia gravis, muscle strength is normal when resting, but true weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions.[3][4][5][6][7][8]

Asthenia vs. myasthenia

Asthenia (asthenopia, characterized by ready fatiguability. Asthenia is also a side effect of some medications and treatments, such as Ritonavir (a protease inhibitor used in HIV treatment), vaccines such as the HPV vaccine Gardasil[9] and fentanyl patches (an opioid used to treat pain).

Differentiating psychogenic (perceived) asthenia and true asthenia from myasthenia is often difficult, and in time apparent psychogenic asthenia accompanying many chronic disorders is seen to progress into a primary weakness.

Myasthenia (my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness"), or simply muscle weakness, is a lack of muscle strength. The causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular diseases, such as myasthenia gravis.

Types

Muscle fatigue can be central, neuromuscular, or peripheral muscular. Central muscle fatigue manifests as an overall sense of energy deprivation, and peripheral muscle weakness manifests as a local, muscle-specific inability to do work.[10][11] Neuromuscular fatigue can be either central or peripheral.

Central fatigue

The central fatigue is generally described in terms of a reduction in the

  • Jun Mapili's Muscle Weakness Coding Checklist
  • AllRefer
  • Unexplained Muscle Weakness - Information About McArdle's Disease

External links

  1. ^ Marx, John (2010). Rosen's Emergency Medicine: Concepts and Clinical Practice (7th ed.). Philadelphia, PA: Mosby/Elsevier. p. Chapter 11.  
  2. ^  
  3. ^ Paul L, Wood L, Behan WM, Maclaren WM (January 1999). "Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome". Eur. J. Neurol. 6 (1): 63–9.  
  4. ^ McCully KK, Natelson BH (November 1999). "Impaired oxygen delivery to muscle in chronic fatigue syndrome". Clin. Sci. 97 (5): 603–8; discussion 611–3.  
  5. ^ De Becker P, Roeykens J, Reynders M, McGregor N, De Meirleir K (November 2000). "Exercise capacity in chronic fatigue syndrome". Arch. Intern. Med. 160 (21): 3270–7.  
  6. ^ De Becker P, McGregor N, De Meirleir K (September 2001). "A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome". J. Intern. Med. 250 (3): 234–40.  
  7. ^ Carruthers, Bruce M.; Jain, Anil Kumar; De Meirleir, Kenny L.; Peterson, Daniel L.; Klimas, Nancy G.; et al. (2003). "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols". Journal of Chronic Fatigue Syndrome 11 (1): 7–115.  
  8. ^ Jammes Y, Steinberg JG, Mambrini O, Brégeon F, Delliaux S (March 2005). "Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise". J. Intern. Med. 257 (3): 299–310.  
  9. ^ Loris McVittie, Ph.D. (June 12, 2008). "Information from CDC and FDA on the Safety of Gardasil Vaccine". Office of Vaccines Research and Review at the US FDA. Retrieved 2008-07-21. We have approved your supplement to your  
  10. ^ Gandevia SC, Enoka RM, McComas AJ, Stuart DG, Thomas CK (1995). "Neurobiology of muscle fatigue. Advances and issues". Adv. Exp. Med. Biol. 384: 515–25.  
  11. ^ Kent-Braun JA (1999). "Central and peripheral contributions to muscle fatigue in humans during sustained maximal effort". European journal of applied physiology and occupational physiology 80 (1): 57–63.  
  12. ^ Gandevia SC (2001). "Spinal and supraspinal factors in human muscle fatigue". Physiol. Rev. 81 (4): 1725–89.  
  13. ^ Kay D, Marino FE, Cannon J, St Clair Gibson A, Lambert MI, Noakes TD (2001). "Evidence for neuromuscular fatigue during high-intensity cycling in warm, humid conditions". Eur. J. Appl. Physiol. 84 (1–2): 115–21.  
  14. ^ Vandewalle H, Maton B, Le Bozec S, Guerenbourg G (1991). "An electromyographic study of an all-out exercise on a cycle ergometer". Archives internationales de physiologie, de biochimie et de biophysique 99 (1): 89–93.  
  15. ^ Bigland-Ritchie B, Woods JJ (1984). "Changes in muscle contractile properties and neural control during human muscular fatigue". Muscle Nerve 7 (9): 691–9.  
  16. ^ Noakes TD (2000). "Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance". Scandinavian journal of medicine & science in sports 10 (3): 123–45.  
  17. ^ Davis JM (1995). "Carbohydrates, branched-chain amino acids, and endurance: the central fatigue hypothesis". Int J Sport Nutr 5 (Suppl): S29–38.  
  18. ^ Newsholme, E. A., Acworth, I. N., & Blomstrand, E. 1987, 'Amino acids, brain neurotransmitters and a functional link between muscle and brain that is important in sustained exercise', in G Benzi (ed.), Advances in Myochemistry, Libbey Eurotext, London, pp. 127-133.
  19. ^ Newsholme EA, Blomstrand E (1995). "Tryptophan, 5-hydroxytryptamine and a possible explanation for central fatigue". Adv. Exp. Med. Biol. 384: 315–20.  
  20. ^ R. Robergs, F. Ghiasvand, D. Parker (2004). "Biochemistry of exercise-induced metabolic acidosis". Am J Physiol Regul Integr Comp Physiol 287 (3): R502–16.  
  21. ^ Sahlin K (1986). "Muscle fatigue and lactic acid accumulation". Acta Physiol Scand Suppl 556: 83–91.  
  22. ^ Kolata, Gina (February 12, 2008). "Finding May Solve Riddle of Fatigue in Muscles". The New York Times. 

References

Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so.

glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesn't actually cause the burning sensation we feel when we exhaust our oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver, which is known as the Cori cycle.

Muscle cells work by detecting a flow of electrical impulses from the brain, which signals them to contract through the release of calcium by the sarcoplasmic reticulum. Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This makes less calcium available for the muscle cell. In addition, the Columbia researchers propose that an enzyme activated by this released calcium eats away at muscle fibers.[22]

Pathophysiology

Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. This can lower the sensitivity of contractile apparatus to calcium ions (Ca2+) but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell. This counters inhibiting effects of potassium ions (K+) on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving K+ as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.

It was once believed that lactic acid build-up was the cause of muscle fatigue.[21] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.

Lactic acid hypothesis

Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the myocytes. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca2+ to stimulate actin and myosin to contract.

The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore, the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed.

Peripheral muscle fatigue during physical work is considered an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigue—affecting a national average of 72% of adults in the work force in 2002. This causes contractile dysfunction that manifests in the eventual reduction or lack of ability of a single muscle or local group of muscles to do work. The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy.[20]

Peripheral muscle fatigue

For extremely powerful contractions that are close to the upper limit of a muscle's ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the muscle's ability to generate force is most strongly limited by nerve’s ability to sustain a high-frequency signal. After an extended period of maximum contraction, the nerve’s signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply ‘stop listening’ and gradually cease to move, often lengthening. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout. Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force. It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force.

Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the muscle that it innervates. Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue.

Neuromuscular fatigue

[19][18][17] pathways.serotonergic The exact mechanisms of central fatigue are unknown, though there has been a great deal of interest in the role of [16][15]

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